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| Main Authors: | , , , , , , , , |
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| Format: | Artículo científico |
| Language: | en |
| Published: |
Fish & shellfish immunology
2026
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| Subjects: | |
| Online Access: | https://pubmed.ncbi.nlm.nih.gov/41319889/ |
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Table of Contents:
- Response mechanisms of abalone Haliotis discus hannai to lead (Pb) exposure in vitro: insights into autophagy, endoplasmic reticulum stress and apoptosis. Liu, Yue Huang, Dong Pan, Mingzhu Li, Xinxin Qin, Gaochan Yu, Xiaojun Zhang, Ze Mai, Kangsen Zhang, Wenbing Animals Lead Autophagy Endoplasmic Reticulum Stress Apoptosis Water Pollutants, Chemical Gastropoda Dose-Response Relationship, Drug The persistence and toxicity of lead (Pb) pose an enduring threat to aquaculture and the ecosystem through bioaccumulation in the food chain. This study investigated the cellular response mechanism induced by Pb in the commercially valuable mollusc, abalone. Initial exposure to a range of Pb concentrations (0, 20, 50, 100, 200, 500, 1000, and 2000 μM) revealed that the cells exhibited adaptability to low concentrations, whereas high concentrations (≥500 μM) significantly damaged cell viability and morphology. Based on these findings, four concentrations (0, 50, 100, and 500 μM) were selected for mechanistic investigation. The results revealed a positive correlation between Pb concentration and the induction of both autophagy and endoplasmic reticulum (ER) stress. Specifically, Pb induced autophagy by suppressing mTOR phosphorylation and p62 protein levels, upregulating the LC3-II/Ⅰ ratio, and increasing the expression of autophagy-related (atg) genes. Increased ER stress was evidenced by elevated mRNA levels of ire, perk and atf4, higher protein level of GRP78, and enhanced xbp1 splicing. Moreover, mitochondrial function and apoptosis levels remained relatively stable at Pb concentrations up to 100 μM, while exposure to the high level of Pb (500 μM) significantly induced mitochondrial dysfunction and triggered cell apoptosis. In conclusion, the present study indicated that autophagy and ER stress function as adaptive mechanisms under mild Pb stress (0-100 μM), while their excessive activation under severe Pb exposure (500 μM) triggered apoptosis, ultimately threatening the survival of cells.